Blood And Lymph- Agents Used In Anemia By Maloney

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Blood and Lymph- Agents Used In Anemia by Maloney

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Blood and Lymph- Agents Used In Anemia by Maloney

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Some requirements for red blood cell production, and what happens if you're low in any of them?

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Iron
-low --> low Hb--> microcytic, hypochromic anemia

Vitamin B12
-low --> reduced DNA synthesis -->megaloblastic anemia
-low --> nerve demylenation and damage

Folic acid
- low --> reduced DNA synthesis --> megaloblastic anemia

Growth factors (Erythropoietin)
-low--> reduced production of RBCs

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Blood and Lymph- Agents Used In Anemia by Maloney

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Blood and Lymph- Agents Used In Anemia by Maloney

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Some requirements for red blood cell production, and what happens if you're low in any of them?

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Iron
-low --> low Hb--> microcytic, hypochromic anemia

Vitamin B12
-low --> reduced DNA synthesis -->megaloblastic anemia
-low --> nerve demylenation and damage

Folic acid
- low --> reduced DNA synthesis --> megaloblastic anemia

Growth factors (Erythropoietin)
-low--> reduced production of RBCs

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Iron Deficiency Anemia causes and treatments

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Cause:
Blood loss
Increased requirement (Pregnancy)
Inadequate iron intake (Dietary insufficiency not common cause;
Generalized intestinal malabsorption)

Tx:
-200 mg elemental iron/day for 3-6 months (so much for so long in order to replace the stores)
-About 50-100 mg of elemental iron can be incorporated into Hb daily
-About 25% of oral iron as ferrous salt can be absorbed

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Iron Parenteral Preps

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Iron Dextran (INFeD, DexFerrum)
-IM or IV
-Absorption slow (up to 2 months) - IM

Iron Sucrose (Venofer)
-IV

Sodium ferric gluconate complex in sucrose (Ferrlecit)
-IV

*use when you have malabsorption, intolerance, chronic blood loss, noncompliance, anemia of chronic renal failure.

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Iron Adverse Effects, oral or intramuscular, IM & IV

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Oral:
GI irritation, nausea, diarrhea or constipation (big thing)

IM:
-Skin discoloration, local inflammation, pain
-Use z-track injection technique

IM & IV:
-Immediate hypersensitivity reaction
-Give small test dose before giving the full dose
-Delayed hypersensitivity reaction - arthralgia, backache, myalgia, fever, chills, dizziness, headache, malaise, nausea, vomiting

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Acute Iron Toxicity, who gets it, why does it happen, what can happen

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-Occurs in children
-Due to its corrosive effects on the GI mucosa
-GI toxicity followed by multiorgan failure

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What are the four stages of Acute Iron Toxicity

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Stage 1 - GI irritation, nausea, vomiting, diarrhea, lassitude, drowsiness, pallor, cyanosis, seizures, shock, coma.

Stage 2 - Apparent recovery (but you're not getting better)

Stage 3 – Multiorgan Failure; CNS (lethargy, coma, convulsions);
Metabolic acidosis; Hepatotoxicity (necrosis); Renal failure (acute tubular necrosis); Susceptibility to bleeding; Cardiovascular collapse (intractable hypotension, pulmonary edema)

Stage 4 – Delayed Effects; Intestinal obstructions; Pyloric stenosis; Hepatic cirrhosis; Severe gastric scarring

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Acute Iron Toxicity Treatment

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Induce vomiting

Gastric lavage

Deferoxamine (Desferal) Iron chelator

Supportive therapy

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Chronic Iron Toxicity...where does the iron go? Causes?

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-Excess iron deposits in the heart, liver, pancreas, pituitary and synovia
-Organ failure & death

-Hereditary hemochromatosis
-Red cell transfusions (eg. With thalassemia major)
-Excess ingestion (In individuals with an underlying disease)

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Treatment of Chronic Iron Toxicity

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-Phlebotomy
-Deferoxamine (Desferal) – IM or IV; iron chelator
-Deferasirox (Exjade) – Oral; iron chelator

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Pharmacokinetics of B12 in stomach, small intestine, liver.

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Vit B12 comes in with food protein, the HCl/pepsin breaks that apart. B12 then binds with R protein (or haptocorrin), so B12-R and then Intrinsic Factor go down to the small intestine...in the intestine, pancreatic proteases break up the B12-R, the B12 then binds with IF, then via an IF receptor, this complex leaves the intestine (is absorbed). Then IF breaks off the B12, TCII attaches on, and via plasma, this B12 goes to the liver for storage.

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Vitamin B12 deficiency causes

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Diet (Strict vegans...only get B12 from animal products)

Drugs (Proton pump inhibitors)

Gastric abnormalities (Pernicious anemia..not making IF; Gastrectomy/bariatric surgery)

Small bowel disease (Crohn’s disease; Ileal resection)

Pancreatitis (can't break R-B12 bond)

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Folic Acid Pharmacokinetics

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Dietary sources are converted to CH3H4PteGlu1 during GI transport

Absorbed in the proximal part of small intestine

Only few day supply in liver

Enterohepatic recirculation

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Causes of Folic Acid Deficiency

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Nutritional deficiency (Poor dietary intake; Chronic alcoholism)

Malabsorption (Sprue; Inflammatory bowel disease)

Drugs

Increased requirement (Pregnancy)

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Pharmacodynamics Of Vitamin B12 and Folic Acid..what do you need it for? What happens if you don't have enough B12?

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Both are required for the production of tetrahydrofolate, which is required for DNA synthesis.

So you need B12 and folate for DNA synthesis. On the other hand, just a deficiency in B12 can affect myelin sheaths of neurons.

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What may happen to homocysteine levels in a patient with a folic acid deficiency?

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it will increase. and too much is bad for you.

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Symptoms of Vitamin B12 deficiency

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-Megaloblastic anemia
-GI problems
-*Demylenation of nerves --> cell death

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B12 deficiency Treatment

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Cyanocobalamin or hydroxocobolamin IM, deep subcutaneous or intranasal

Usually for life

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Folic Acid Deficiency symptoms

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megaloblastic anemia
-no neurological problems

treat with oral folic acid.

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Hematopoietic Growth Factors Agents (6)

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Epoetin alfa (Epogen, Procrit, Eprex) ; Erythropoietin

Darbepoetin Alfa (Aranesp); Analog of erythropoietin with longer half life

Sargramostim (Leukine) - GM-CSF

Filgrastim (Neupogen) - G-CSF

Pegfilgrastim (Neulasta)
-Covalent conjugate of filgrastim and monomethoxypolyethylene glycol (PEG); Delays renal clearance to increase half life of filgrastim

Oprelvekin (Neumega) - IL-11

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Epoetin alfa and Darbepoetin Alfa-->

Sargramostim; Filgrastim; Pegfilgrastim-->

Oprelvekin-->

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--> increase Red blood cells (chemo to treat anemia)

--> increase neutrophils (chemo to treat neutropenia)

--> increase platelets (chemo to treat thrombocytopenia)

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Why would you get anemia with chronic renal failure?

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erythropoetin is made in the kidney